The significance of cell death by apoptosis in hepatobiliary disease

Searle, Jeffrey; Harmon, Brian V.; Bishop, C. J.; Kerr, Judith

doi:10.1111/j.1440-1746.1987.tb00152.x

Cited by 91 publications

(43 citation statements)

References 53 publications

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“…However, widespread hepatocyte necrosis is not a prominent feature of cholestatic liver disease. In contrast, cell dropout associated with acidophilic bodies is frequently identified in human cholestatic liver disease (8). These histopathologic findings are now recognized as morphologic features of cell death by a process referred to as apoptosis (8).…”

Section: Introductionmentioning

confidence: 99%

“…Later, the cell fragments into membrane-bound fragments. These cell fragments, traditionally referred to as acidophilic bodies in the liver, are now termed apoptotic bodies (8). The biochemical mechanisms of apoptosis leading to these morphologic changes remain unclear.…”

Section: Introductionmentioning

confidence: 99%

“…In addition to its physiological role in normal cell turnover as well as regression of liver hyperplasia (8,12), apoptosis contributes to hepatocyte cytotoxicity by toxins. Various hepatotoxins such as 1, l,dichloroethylene, dimethylnitrosamine, and cis-platinum have all been shown to cause liver injury by apoptosis (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

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Increases of intracellular magnesium promote glycodeoxycholate-induced apoptosis in rat hepatocytes.

Patel¹,

Bronk²,

Gores³

1994

J. Clin. Invest.

258

172

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Increases of intracellular magnesium promote glycodeoxycholate-induced apoptosis in rat hepatocytes.

Patel¹,

Bronk²,

Gores³

1994

J. Clin. Invest.

258

172

View full text Add to dashboard Cite

show abstract

“…Comparatively little is known about the contribution of apoptosis to the ischemic lesions of the liver. [23][24][25][26] In particular, the contribution of apoptosis to the lesions of hypoxiareperfusion presented by liver allografts at the end of the transplantation procedure have not been explored. To address this question, we analyzed 16 postoperative biopsy specimens of liver allografts using the TUNEL assay.…”

confidence: 99%

Apoptosis after ischemia-reperfusion in human liver allografts

et al. 1997

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Little is known about the possible contribution of apoptosis to ischemia-reperfusion injury in human liver transplantation. Therefore, we studied postreperfusion surgical biopsy specimens of 16 human liver allografts using the TUNEL assay for in situ demonstration of apoptotic cells. In all patients, a variable proportion of hepatocytes and sinusoidal endothelial cells presented labeled nuclei. The mean ؎ standard deviation percentages of positive hepatocytes were 18.7% ؎ 12.2% in the whole section, 30.4% ؎ 18.7% in the subcapsular region, 14.5% ؎ 13.5% in the centrilobular zones, and 10.3% ؎ 9.5% in the periportal zones. The percentage of positive hepatocytes were not correlated with the duration of cold ischemia but was higher in grafts harvested from donors with elevated preoperative aspartate aminotransferase (AST) levels. The percentage of positive hepatocytes was correlated with postoperative serum levels of AST (P ‫؍‬ .015) and inversely correlated with postoperative serum levels of factor V (P ‫؍‬ .019). Apoptotic biliary epithelial cells were detected in only 3 cases. In conclusion, apoptosis is a frequent event in postreperfusion biopsy specimens of liver allografts and probably contributes to preservation injury of hepatocytes.

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“…These latter appearances of course represent apoptosis of hepatocytes, recognized by Kerr [38] some 30-40 years before but not widely appreciated until interest developed in the 1980s in the apoptosis process. A detailed analysis of apoptosis in the context of chronic hepatitis and liver cell degeneration is given by Searle et al [39] . There were two morphological features additional to those described by Klatskin that deserve comment.…”

Section: Pathological Features Of Chronic Active/aihmentioning

confidence: 99%

Historical reflections on autoimmune hepatitis

Mackay

2008

WJG

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Autoimmune hepatitis (AIH), initially known as chronic active or active chronic hepatitis (and by various other names), first came under clinical notice in the late 1940s. However, quite likely, chronic active hepatitis (CAH) had been observed prior to this and was attributed to a persistently destructive virus infection of the liver. An earlier (and controversial) designation in 1956 as lupoid hepatitis was derived from associated L.E. cell test positivity and emphasized accompanying multisystem features and immunological aberrations. Yo u n g w o m e n f e a t u r e d p r o m i n e n t l y i n e a r l y descriptions of CAH. AIH was first applied in 1965 as a descriptive term. Disease-characteristic autoantibodies were defined from the early 1960s, notably antinuclear antibody (ANA), smooth muscle antibody (SMA) and liver-kidney microsomal (LKM) antibody. These are still widely used diagnostically but their relationship to pathogenesis is still not evident. A liver and disease specific autoantigen has long been searched for but unsuccessfully. Prolonged immunosuppressive therapy with prednisolone and azathioprine in the 1960s proved beneficial and remains standard therapy today. AIH like many other autoimmune diseases is associated with particular HLA alleles especially with the "ancestral" B8, DR3 haplotype, and also with DR4. Looking forwards, AIH is one of the several enigmatic autoimmune diseases that, despite being (relatively) organ specific, are marked by autoimmune reactivities with non-organ-specific autoantigens. New paradigms are needed to explain the occurrence, expressions and pathogenesis of such diseases.

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The significance of cell death by apoptosis in hepatobiliary disease

Cited by 91 publications

References 53 publications

Increases of intracellular magnesium promote glycodeoxycholate-induced apoptosis in rat hepatocytes.

Increases of intracellular magnesium promote glycodeoxycholate-induced apoptosis in rat hepatocytes.

Apoptosis after ischemia-reperfusion in human liver allografts

Historical reflections on autoimmune hepatitis

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